ArticleJournal of inflammation research2013
Knockout of the c-Jun N-terminal Kinase 2 aggravates the development of mild chronic dextran sulfate sodium colitis independently of expression of intestinal cytokines TNFα, TGFB1, and IL-6.
Article in Journal of inflammation research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- The JNK2-microbiome axis modulates gut barrier integrity through microbial acetate.Gut microbes · 2026Article
- Clostridium butyricum Regulates the Inflammatory and Immunoregulatory Pathway Through NFKB1 in Colorectal Cancer Treatment.Probiotics and antimicrobial proteins · 2026Article
- Design, synthesis and biological evaluation of novel O-substituted tryptanthrin oxime derivatives as c-JunFrontiers in pharmacology · 2022Article
- The lipid peroxidation product EKODE exacerbates colonic inflammation and colon tumorigenesis.Redox biology · 2021Article
- Genome-wide association study of an unusual dolphin mortality event reveals candidate genes for susceptibility and resistance to cetacean morbillivirus.Evolutionary applications · 2019Article
- Role of pregnane X-receptor in regulating bacterial translocation in chronic liver diseases.World journal of hepatology · 2017Review
- c-Jun N-terminal kinase 2 promotes enterocyte survival and goblet cell differentiation in the inflamed intestine.Mucosal immunology · 2017Article
- Pregnane X Receptor Activation Attenuates Inflammation-Associated Intestinal Epithelial Barrier Dysfunction by Inhibiting Cytokine-Induced Myosin Light-Chain Kinase Expression and c-Jun N-Terminal Kinase 1/2 Activation.The Journal of pharmacology and experimental therapeutics · 2016Article
- Jnk2 deletion disrupts intestinal mucosal homeostasis and maturation by differentially modulating RNA-binding proteins HuR and CUGBP1.American journal of physiology. Cell physiology · 2014Article
- The impact of JNK inhibitor D-JNKI-1 in a murine model of chronic colitis induced by dextran sulfate sodium.Journal of inflammation research · 2013Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe c-Jun N-terminal kinases (JNKs) are involved in signal transduction of inflammatory bowel diseases. The aim of this study was to examine the function of JNKs by using a low-dose dextran sulfate sodium (DSS) model in JNK1 knockout mice (Mapk8-/-), JNK2 knockout mice (Mapk9-/-), and wild-type controls (WT1, WT2).
methodsThe animals were evaluated daily using a disease activity index. After 30 days, the intestine was evaluated histologically with a crypt damage score. CD4+ and CD8+ cells were quantified using immunofluorescence. Analysis of tumor necrosis factor-α (TNFα), interleukin-6 (IL-6), and transforming growth factor β1 (TGFB1) expression was carried out using LightCycler(®) real-time polymerase chain reaction.
resultsCyclic administration of low-dose DSS (1%) was not able to induce features of chronic colitis in Mapk8-/- WT2 mice. By contrast, DSS administration significantly increased the disease activity index in WT1 and Mapk9-/- mice. In Mapk9-/- mice, the crypt damage score and the number of CD4+ and CD8+ cells as features of chronic colitis/inflammation were also significantly elevated. Expression of TNFα, IL-6, and TGFB1 was not altered by the JNK knockout.
conclusionAdministering DSS at a defined low concentration that is unable to induce colitis in WT animals leads to clinically and histologically detectable chronic colitis in Mapk9-/- mice. The reason for this disease-inducing effect resulting from the loss of JNK2 remains to be elucidated. Expression of TNFα, IL-6, and TGFB1 does not appear to be involved; proapoptotic JNK2 may prolong the activity of proinflammatory immune cells, leading to perpetuation of the inflammation.
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